Respiratory Effects of Breathing High Oxygen During Incremental Exercise in Humans

Abstract

During incremental exercise to exhaustion, minute ventilation (V E) increases in a linear manner with respect to work rate, oxygen consumption (VO2) and carbon dioxide production (VC02), until a threshold level of work rate. After this point, the slope of the VE/work rate relationship is steeper than it was at lower work rates. This point is known as the ventilatory anaerobic threshold (VAT). At approximately the same threshold work rate, blood lactate concentration begins to rise significantly from its resting level (the lactate anaerobic threshold, LAT), and this may or may not be causally related to the VAT. Wasserman et al.1 have argued that lactic acidosis contributes to an additional component of the ventilatory response via stimulation of the peripheral chemoreceptors, and that this is an adaptive response in which the ensuing respiratory alkalosis limits the fall in pH generated by metabolic acidosis. Consistent with this hypothesis, it has been observed that subjects who have undergone carotid body resection do not show the characteristic slope of the VE/work rate relationship above the anaerobic threshold and lose the inflection point of the VAT1. However, subjects with McArdle’s syndrome (myophosphorylase deficiency) produce no lactic acid and hence lack a lactate anaerobic threshold, but they nonetheless demonstrate a ventilatory anaerobic threshold2. Paterson et al.3 have argued that arterial plasma potassium (K+), rather than lactic acid, contributes to the hyperventilation above VAT in these (and perhaps also in normal) subjects. Regardless of whether K+ or lactate is the chemical stimulus to the extra ventilation above VAT, there is general agreement that both these stimuli act via the final common pathway of the carotid bodies.